Interleukin 1 beta (IL-1b) is a highly potent bone resorptive cytokine which is responsible for most of the activity formerly referred to as osteoclast activating factor, or `OAF` (Dewhirst et al. 1985). IL-1b is produced in large amounts by macrophage-monocytes in response to a variety of stimuli, including bacterial components such as LPS (Burchett et al. 1988). IL-1b exerts other biological activities consistent with its potential role as a local mediator of tissue destruction in human periodontitis. These include inhibition of bone formation (Stashenko et al. 1987, Nguyen et al. 1990), stimulation of prostaglandin and thromboxane synthesis (Tatakis 1988), stimulation of collagenase and protease production (Mizel et al. 1981, Saklatvala et al. 1985), potentiation of neutrophil degranulation and superoxide production (Dinarello 1989), enhancement of endothelial cell-leukocyte adhesion (Bevilacqua et al. 1987), and stimulation of fibroblast and keratinocyte proliferation (Schmidt et al. 1982). IL-1-like activity is present in elevated amounts in crevicular fluid adjacent to sites of gingival inflammation (Charon et al. 1982). Recently IL-1 b-containing cells were shown to be present in greater numbers in diseased as compared to clinically-healthy periodontal tissues (Jandinski et al. 1990).
Substantial evidence indicates that periodontal destruction is not continuous, but rather occurs episodically in bursts of disease activity (Goodson et al. 1982). At any given point in time the majority of sites with periodontal disease involvement are in fact quiescent. An important consequence of this finding is that putative host or bacterial indicators of periodontal disease must be evaluated in the temporal context of these relatively infrequent events (Caton 1990). It is therefore desirable to provide an effective method of determining periodontal disease active sites in the oral cavity of a patient.